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10.1093/ndtplus/sfr164 http://scihub22266oqcxt.onion/10.1093/ndtplus/sfr164 26069817!4455826!26069817     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Clin+Kidney+J 2012 ; 5 (Suppl 1): i15-i24 Nephropedia Template TP {{tp|p=26069817|t=2012. Regulation of magnesium balance: lessons learned from human genetic disease |pdf=|usr=}}{{26069817}} gab.com Text Regulation of magnesium balance: lessons learned from human genetic disease JO: Clin Kidney J http://www.kidney.de/pget.php?&tw=1&pmid=26069817 #FOAvip Magnesium (Mg(2+)) is the fourth most abundant cation in the body. Thus, magnesium homeostasis needs to be tightly regulated, and this is facilitated by intestinal absorption and renal excretion. Magnesium absorption is dependent on two concomitant pathways found in both in the intestine and the kidneys: passive paracellular transport via claudins facilitates bulk magnesium absorption, whereas active transcellular pathways mediate the fine-tuning of magnesium absorption. The identification of genes responsible for diseases associated with hypomagnesaemia resulted in the discovery of several magnesiotropic proteins. Claudins 16 and 19 form the tight junction pore necessary for mass magnesium transport. However, most of the causes of genetic hypomagnesaemia can be tracked down to transcellular magnesium transport in the distal convoluted tubule. Within the distal convoluted tubule, magnesium reabsorption is a tightly regulated process that determines the final urine magnesium concentration. Therefore, insufficient magnesium transport in the distal convoluted tubule owing to mutated magnesiotropic proteins inevitably leads to magnesium loss, which cannot be compensated for in downstream tubule segments. Better understanding of the molecular mechanism regulating magnesium reabsorption will give new opportunities for better therapies, perhaps including therapies for patients with chronic renal failure. Twit Text FOAVip Regulation of magnesium balance: lessons learned from human genetic disease ????Clin Kidney J http://www.kidney.de/pget.php?&tw=1&pmid=26069817 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26069817 #FOAvip English Wikipedia <ref>{{Cite pmid|26069817}}</ref> Regulation of magnesium balance: lessons learned from human genetic disease #MMPMID26069817 de Baaij JH; Hoenderop JG; Bindels RJ Clin Kidney J 2012[Feb]; 5 (Suppl 1): i15-i24 PMID26069817show ga Magnesium (Mg(2+)) is the fourth most abundant cation in the body. Thus, magnesium homeostasis needs to be tightly regulated, and this is facilitated by intestinal absorption and renal excretion. Magnesium absorption is dependent on two concomitant pathways found in both in the intestine and the kidneys: passive paracellular transport via claudins facilitates bulk magnesium absorption, whereas active transcellular pathways mediate the fine-tuning of magnesium absorption. The identification of genes responsible for diseases associated with hypomagnesaemia resulted in the discovery of several magnesiotropic proteins. Claudins 16 and 19 form the tight junction pore necessary for mass magnesium transport. However, most of the causes of genetic hypomagnesaemia can be tracked down to transcellular magnesium transport in the distal convoluted tubule. Within the distal convoluted tubule, magnesium reabsorption is a tightly regulated process that determines the final urine magnesium concentration. Therefore, insufficient magnesium transport in the distal convoluted tubule owing to mutated magnesiotropic proteins inevitably leads to magnesium loss, which cannot be compensated for in downstream tubule segments. Better understanding of the molecular mechanism regulating magnesium reabsorption will give new opportunities for better therapies, perhaps including therapies for patients with chronic renal failure. äRegulation of magnesium balance: lessons learned from human genetic di(epmc).pdf DeepDyve Pubget Overpricing